Vitamin K Deficiency Bleeding in Infancy

Newborn infants present a special problem with respect to vitamin K. They have low plasma levels of prothrombin and the other vitamin K-dependent clotting factors (about 30% to 60% of the adult concentrations, depending on gestational age). To a great extent, this is the result of the relatively late development of liver glutamate carboxylase, but they are also short of vitamin K, as a result of the placental barrier that limits fetal uptake of the vitamin. This is probably a way of regulating the activity of Gas6 and other vitantin K-dependent proteins in development and differentiation (Section 5.3.4 Israels et al., 1997). 

Over the first 6 weeks of postnatal life, the plasma concentrations of clotting factors gradually rise to the adult level in the meantime, they are at risk of potentially fatal hemorrhage that was formerly called hemorrhagic disease of the newborn and is now known as vitamin K deficiency bleeding in infancy. It is usual to give all newborn infants prophylactic vitamin K, either orally or by intramuscular injection (Sutor et al., 1999). At one time, menadione was used, but, because of the association between menadione and childhood leukemia (Section 5.6.1), phylloquinone is preferred. 

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Menadione prophylaxis against vitamin K deficiency bleeding in infancy (Section 5.4.1) has been associated with increased incidence of childhoodleukemia and other cancers. 

Sutor AH, von Kries R, Cornelissen EA, McNinch AW, and Andrew M (1999) Vitamin K deficiency bleeding (VKDB) in infancy. ISTH Pediatric/Perinatal Subcommittee. International Society on Thrombosis and Haemostasis. Thrombosis and Haemostasis 81,456-61. 

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